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Ocular Ischemic Diseases: From Molecular Mechanisms to Therapeutics
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Ocular Ischemic Diseases: From Molecular Mechanisms to Therapeutics

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (20 August 2025) | Viewed by 5790

Special Issue Editor

Dr. Deokho Lee

E-Mail Website
Guest Editor
Laboratory of Photobiology, Keio University School of Medicine, Tokyo 160-8582, Japan
Interests: neuroprotection; ischemia; hypoxia; neovascularization; macular degeneration; stroke; glucose and lipid metabolism; oxidative stress; anti-aging; nicotinamide adenine dinucleotide; vitamin supplements; hypoxia-inducible factors
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Ocular ischemia is one of the leading causes of visual loss. Many eye diseases, including diabetic retinopathy, retinopathy of prematurity, retinal vein/artery occlusion, pathologic myopia, age-related macular degeneration, glaucoma, and ocular ischemic syndrome, are highly related to ocular ischemia. To develop or find promising preventive or protective drugs in ocular ischemic diseases, the complex molecular mechanisms of pathologies in ocular ischemia need to first be well understood.

This Special Issue aims to collect original research and review articles that summarize recent state-of-the-art findings, focusing on unravelling the pathologic molecular pathways in various types of ocular ischemic diseases and suggesting novel therapeutic molecular targets in terms of the prevention and treatment of ocular ischemia.

Topics include, but are not limited to, the following:

  • Diabetic retinopathy.
  • Retinopathy of prematurity.
  • Retinal vein occlusion.
  • Retinal artery occlusion.
  • Pathologic myopia.
  • Age-related macular degeneration.
  • Glaucoma.
  • Ocular ischemic syndrome.

Dr. Deokho Lee
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • diabetic retinopathy
  • retinopathy of prematurity
  • retinal vein occlusion
  • retinal artery occlusion
  • pathologic myopia
  • age-related macular degeneration
  • glaucoma
  • ocular ischemic syndrome

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Published Papers (3 papers)

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Research

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18 pages, 4790 KB  
Article
Tonabersat Inhibits Retinal Inflammation After Hypoxia–Ischemia in the Neonatal Rat
by Jack Jonathan Maran, Alice McDouall, Justin M. Dean, Joanne Davidson and Odunayo O. Mugisho
Int. J. Mol. Sci. 2025, 26(16), 7996; https://doi.org/10.3390/ijms26167996 - 19 Aug 2025
Viewed by 184
Abstract
Perinatal hypoxic–ischemic encephalopathy (HIE) is a condition resulting from oxygen deprivation around the time of birth and may be associated with death, brain damage, and disability. Alongside this, studies have shown that HIE may result in visual impairment. Previously, this was thought to [...] Read more.
Perinatal hypoxic–ischemic encephalopathy (HIE) is a condition resulting from oxygen deprivation around the time of birth and may be associated with death, brain damage, and disability. Alongside this, studies have shown that HIE may result in visual impairment. Previously, this was thought to be due to damage to the visual pathways in the brain, in a condition known as cerebral visual impairment. However, recent studies suggest that direct injury to the retina may occur after HIE. Of note, the nucleotide-binding domain, leucine-rich-containing family, and pyrin domain-containing-3 (NLRP3) inflammasome is thought to play a role in perpetuating inflammatory damage in the brain after hypoxia–ischemia (HI). As such, this study aimed to characterize retinal inflammation and the role of the NLRP3 inflammasome after HI using a modified Rice-Vannucci model in postnatal day 10 (P10) rat. Eighteen Sprague-Dawley rats were allocated evenly to three groups. Two groups received surgery to ligate the right common-carotid artery and induce HI, while another group received only sham surgery. Rats exposed to HI received subcutaneous injections of tonabersat (HI + Ton) or saline (HI + vehicle) at 1, 24 and 48 h after HI, and were culled at P17 for analysis. The results showed that the protein expression of GFAP, Iba-1, NLRP3, caspase-1 and connexin43 increased in the retina at 7 d after HI-vehicle compared with sham surgery, much more so in the ipsilateral = than the contralateral retina. Furthermore, = inflammasome components NLRP3, cleaved caspase-1 and connexin43 were significantly upregulated in the ipsilateral retina following HI-vehicle compared to the sham surgery group. Treatment with a connexin43 hemichannel blocker, tonabersat, significantly decreased the expression of the inflammasome markers, cleaved caspase-1 and connexin43, and diminished Iba-1+ cell infiltration in the ipsilateral retina. These findings suggest that direct retinal damage and inflammation may occur after HI. Furthermore, these inflammatory changes are likely mediated and propagated by activation of the NLRP3 inflammasome. Importantly, inhibition of the inflammasome by tonabersat may be able to inhibit retinal inflammation and damage, potentially preventing visual impairment after HI. Further investigation in humans is required to determine the efficacy of tonabersat in treating hypoxic–ischemic injuries to the brain and eye. Full article
(This article belongs to the Special Issue Ocular Ischemic Diseases: From Molecular Mechanisms to Therapeutics)
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Review

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14 pages, 767 KB  
Review
Interplay Between Ocular Ischemia and Glaucoma: An Update
by Valeria Coviltir, Miruna Gabriela Burcel, George Baltă and Maria Cristina Marinescu
Int. J. Mol. Sci. 2024, 25(22), 12400; https://doi.org/10.3390/ijms252212400 - 19 Nov 2024
Cited by 3 | Viewed by 1654
Abstract
Glaucoma is a main cause of irreversible blindness worldwide, with a high impact on productivity and quality of life. The mechanical and ischemic theories are currently the most recognized pathophysiological pathways that explain the neurodegeneration of retinal nerve fibers in glaucoma. In this [...] Read more.
Glaucoma is a main cause of irreversible blindness worldwide, with a high impact on productivity and quality of life. The mechanical and ischemic theories are currently the most recognized pathophysiological pathways that explain the neurodegeneration of retinal nerve fibers in glaucoma. In this narrative review, aspects of ischemia in glaucoma are discussed, including vascular dysregulation, retinal ischemia signaling pathways, roles of vascular endothelial growth factors, and future research and therapeutic directions. In conclusion, a better understanding of the ischemic processes in glaucoma may lead to innovative treatment options and improved management and follow-up of our patients. Full article
(This article belongs to the Special Issue Ocular Ischemic Diseases: From Molecular Mechanisms to Therapeutics)
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13 pages, 1140 KB  
Review
Recent Insights into Roles of Hypoxia-Inducible Factors in Retinal Diseases
by Deokho Lee, Yohei Tomita, Yukihiro Miwa, Hiromitsu Kunimi, Ayaka Nakai, Chiho Shoda, Kazuno Negishi and Toshihide Kurihara
Int. J. Mol. Sci. 2024, 25(18), 10140; https://doi.org/10.3390/ijms251810140 - 21 Sep 2024
Cited by 7 | Viewed by 2961
Abstract
Hypoxia-inducible factors (HIFs) are transcriptional factors that function as strong regulators of oxygen homeostasis and cellular metabolisms. The maintenance of cellular oxygen levels is critical as either insufficient or excessive oxygen affects development and physiologic and pathologic conditions. In the eye, retinas have [...] Read more.
Hypoxia-inducible factors (HIFs) are transcriptional factors that function as strong regulators of oxygen homeostasis and cellular metabolisms. The maintenance of cellular oxygen levels is critical as either insufficient or excessive oxygen affects development and physiologic and pathologic conditions. In the eye, retinas have a high metabolic demand for oxygen. Retinal ischemia can cause visual impairment in various sight-threating disorders including age-related macular degeneration, diabetic retinopathy, and some types of glaucoma. Therefore, understanding the potential roles of HIFs in the retina is highly important for managing disease development and progression. This review focuses on the physiologic and pathologic roles of HIFs as regulators of oxygen homeostasis and cellular metabolism in the retina, drawing on recent evidence. Our summary will promote comprehensive approaches to targeting HIFs for therapeutic purposes in retinal diseases. Full article
(This article belongs to the Special Issue Ocular Ischemic Diseases: From Molecular Mechanisms to Therapeutics)
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